Enhancement of the upper critical field and a field-induced superconductivity in antiferromagnetic conductors

We propose a mechanism by which the paramagnetic pair-breaking effect is largely reduced in superconductors with coexisting antiferromagnetic long- range and short-range orders. The mechanism is an extension of the Jaccarino and Peter mechanism to antiferromagnetic conductors, but the resultant phase diagram is quite different. In order to illustrate the mechanism, we examine a model which consists of mobile electrons and antiferromagnetically correlated localized spins with Kondo coupling between them. It is found that for weak Kondo coupling, the superconductivity occurs over an extraordinarily wide region of the magnetic field including zero field. The critical field exceeds the Chandrasekhar and Clogston limit, but there is no lower limit in contrast to the Jaccarino and Peter mechanism. On the other hand, for strong Kondo coupling, both the low-field superconductivity and a field-induced superconductivity occur. Possibilities in hybrid ruthenate cuprate superconductors and some organic superconductors are discussed.Comment: 5 pages, 1 figure, revtex.sty, to be published in J.Phys.Soc.Jpn. Vol.71, No.3 (2002

Ferromagnetism and Superconductivity in Uranium Compounds

Recent advances on ferromagnetic superconductors, UGe2, URhGe and UCoGe are presented. The superconductivity (SC) peacefully coexists with the ferromagnetism (FM), forming the spin-triplet state of Cooper pairs. The striking new phenomena, such as SC reinforced by the magnetic field, are associated with Ising-type ferromagnetic fluctuations. A variety of ferromagnetic ordered moments between UGe2, URhGe and UCoGe affords to understand the relation between FM, tricriticality and SC.Comment: 11 pages, 16 figures, accepted for publication in J. Phys. Soc. Jpn. as a review article of Special Topics of "Recent developments in superconductivity

A large ozone-circulation feedback and its implications for global warming assessments.

State-of-the-art climate models now include more climate processes which are simulated at higher spatial resolution than ever1. Nevertheless, some processes, such as atmospheric chemical feedbacks, are still computationally expensive and are often ignored in climate simulations1,2. Here we present evidence that how stratospheric ozone is represented in climate models can have a first order impact on estimates of effective climate sensitivity. Using a comprehensive atmosphere-ocean chemistry-climate model, we find an increase in global mean surface warming of around 1°C (~20%) after 75 years when ozone is prescribed at pre-industrial levels compared with when it is allowed to evolve self-consistently in response to an abrupt 4×CO2 forcing. The difference is primarily attributed to changes in longwave radiative feedbacks associated with circulation-driven decreases in tropical lower stratospheric ozone and related stratospheric water vapour and cirrus cloud changes. This has important implications for global model intercomparison studies1,2 in which participating models often use simplified treatments of atmospheric composition changes that are neither consistent with the specified greenhouse gas forcing scenario nor with the associated atmospheric circulation feedbacks3-5.We thank the European Research Council for funding through the ACCI project, project number 267760. The model development was part of the QESM-ESM project supported by the UK Natural Environment Research Council (NERC) under contract numbers RH/H10/19 and R8/H12/124. We acknowledge use of the MONSooN system, a collaborative facility supplied under the Joint Weather and Climate Research Programme, which is a strategic partnership between the UK Met Office and NERC. A.C.M. acknowledges support from an AXA Postdoctoral Research Fellowship.This is the accepted manuscript. The final version is available from Nature Publishing at http://www.nature.com/nclimate/journal/v5/n1/full/nclimate2451.html

A Participatory Approach to Assessing the Climate-Smartness of Agricultural Interventions: The Lushoto Case

The concept of climate-smart agriculture (CSA) is gaining momentum across the globe. However, it is not specific on what should be covered under its three pillars—productivity, resilience and mitigation. Consequently, CSA encompasses many different agricultural practices/technologies, making it difficult to prioritise CSA objectives. Firstly, there is a lack of clear and workable criteria as well as methods for assessing the climate-smartness of interventions. Secondly, little information exists about the impact of the various interventions already promoted as CSA, especially in the developing world. Finally, CSA prioritisation does not take into account stakeholders’ perspectives to ensure that the interventions are applicable, suitable and of high adoption-potential. Here, we describe a new participatory protocol for assessing the climate-smartness of agricultural interventions in smallholder practices. This identifies farm-level indicators (and indices) for the food security and adaptation pillars of CSA. It also supports the participatory scoring of indicators, enabling baseline and future assessments of climate-smartness to be made. The protocol was tested among 72 farmers implementing a variety of CSA interventions in the climate-smart village of Lushoto, Tanzania. Farmers especially valued interventions that improved soil fertility and structure, reduced surface runoff, and reclaimed degraded land due to the positive impacts on yield and off-season crop agriculture. Mostly, the CSA interventions increased animal production, food production, consumption and income. The protocol is easy to adapt to different regions and farming systems and allows for the better prioritisation of interventions. But we recommend that CSA is adopted as part of a monitoring, evaluation and learning process

Exploring the proteasome system: A novel concept of proteasome inhibition and regulation.

The proteasome is a well-identified therapeutic target for cancer treatment. It acts as the main protein degradation system in the cell and degrades key mediators of cell growth, survival and function. The term "proteasome" embraces a whole family of distinct complexes, which share a common proteolytic core, the 20S proteasome, but differ by their attached proteasome activators. Each of these proteasome complexes plays specific roles in the control of cellular function. In addition, distinct proteasome interacting proteins regulate proteasome activity in subcellular compartments and in response to cellular signals. Proteasome activators and regulators may thus serve as building blocks to fine-tune proteasome function in the cell according to cellular needs.Inhibitors of the proteasome, e.g. the FDA approved drugs Velcade (TM), Kyprolis (TM), Ninlaro (TM), inactivate the catalytic 20S core and effectively block protein degradation of all proteasome complexes in the cell resulting in inhibition of cell growth and induction of apoptosis. Efficacy of these inhibitors, however, is hampered by their pronounced cytotoxic side-effects as well as by the emerging development of resistance to catalytic proteasome inhibitors. Targeted inhibition of distinct buiding blocks of the proteasome system, i.e. proteasome activators or regulators, represents an alternative strategy to overcome these limitations.In this review, we stress the importance of the diversity of the proteasome complexes constituting an entire proteasome system. Our building block concept provides a rationale for the defined targeting of distinct proteasome super-complexes in disease. We thereby aim to stimulate the development of innovative therapeutic approaches beyond broad catalytic proteasome inhibition

Metformin induces resistance of cancer cells to the proteasome inhibitor bortezomib.

The anti-diabetic drug metformin is currently tested for the treatment of hematological and solid cancers. Proteasome inhibitors, e.g., Bortezomib, are approved for the treatment of multiple myeloma and mantle cell lymphoma but are also studied for lung cancer therapy. We here analyzed the interaction of the two drugs in two cell lines, namely the mantle cell lymphoma Jeko-1 and the non-small-cell lung cancer (NSCLC) H1299 cells, using proliferation and survival assays, native-gel analysis for proteasome activity and assembly, and expression analysis of proteasome assembly factors. Our results demonstrate that metformin treatment induces resistance of cancer cells to the proteasome inhibitor Bortezomib by impairing the activity and assembly of the 26S proteasome complexes. These effects of metformin on proteasome inhibitor sensitivity in cancer cells are of potential relevance for patients that receive proteasome inhibitor therapy

In-gel proteasome assay to determine the activity, amount, and composition of proteasome complexes from mammalian cells or tissues.

This protocol describes an easy and reliable in-gel proteasome assay to quantify the activity and composition of different proteasome complexes in cells and tissues. The assay works well with limited amounts of total cell protein lysates. Although this assay is optimized specifically for the proteasome chymotrypsin-like activity, it can be expanded to other proteasome activities as well. Using antibodies that detect distinct proteasome subunits or regulators, we can determine the composition and relative quantity of active proteasome complexes. For complete details on the use and execution of this protocol, please refer to Meul et al. (2020)